Dr. David H. Gutmann

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  www.hcnd.org/index.php?option=com_directory&task=view&d - [Cached Version]
  Published on: 6/23/2008    Last Visited: 6/23/2008  

  David H. GutmannHope Center for Neurological Disorders
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  David H. Gutmann

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  www.hcnd.org/bio5663/index.php - [Cached Version]
  Last Visited: 6/23/2008  

  David Gutmann, MD, PhDDepartment: NeurologyResearch Area: Brain Tumor Pathophysiology and Treatment
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  David Gutmann, MD,PhD

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  www.eurekalert.org/pub_releases/2008-08/wuso-gne081108. - [Cached Version]
  Published on: 8/11/2008    Last Visited: 8/12/2008  

  "We've learned that the NF1 gene affects stature through a different pathway than the one we've previously focused on to understand cancers in patients with neurofibromatosis type 1," says Washington University neurologist David H. Gutmann, M.D., Ph.D., a Washington University neurologist who treats individuals with neurofibromatosis at St. Louis Children's Hospital.
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  "We wanted to know if we could blame this on RAS protein activity, so we generated new mice with normal levels of neurofibromin expression, but increased levels of RAS activation in brain stem cells," says Gutmann, the Donald O. Schnuck Family Professor of Neurology, and director of Washington University Neurofibromatosis Center."However, those mice were normal."
  
  NF1 also increases brain levels of cyclic AMP (cAMP), an important signaling molecule.Working with the same line of mice where stem cells in the brain do not make the NF1 protein, researchers fed pregnant mice and their newborns an agent that increased cAMP levels.The baby mice were closer to normal size, even though they still lacked neurofibromin in brain stem cells.Gutmann suspects the mice didn't completely return to normal because dietary supplementation of cAMP levels cannot match the natural ability of neurofibromin to control cAMP levels.
  
  Gutmann is intrigued by the connection to cAMP.Research in other disorders has begun to build a number of associations between cAMP and tumor formation.Gutmann's laboratory and others have treatments in the works for neurofibromatosis 1 that restore the inhibitory effect neurofibromin normally has on RAS, but the new results may mean treatments are also needed to restore neurofibromin's effects on cAMP levels.
  
  "What we've learned also may help us gain insight into other disease processes," Gutmann notes."There are a number of other rare genetic abnormalities that cause short stature, and this same pathway may be involved."
  
  To follow up, Gutmann plans additional studies to explore the role of the NF1 gene in the pituitary gland and the hypothalamus, a brain region that controls pituitary gland production of growth hormone.

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  www.ctf.org/for-scientists/medical-podcasts/ - [Cached Version]
  Published on: 2/13/2008    Last Visited: 2/13/2008  

  Dr. David Gutmann, Washington University School of Medicine, St, LouisDr. Gutmann focuses on the optic glioma tumors of NF1, their diagnosis and clinical management, and what NF1 patients affected by optic pathway glioma need to know.Dr. Gutmann also reviews current and emerging treatments and drug therapies for optic pathway glioma.Finally, Dr. Gutmann discusses the recently launched Children's Tumor Foundation NF Preclinical Consortium to identify drug treatments for NF in which his laboratory participates.

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  www.eurekalert.org/pub_releases/2007-10/wuis-sse101507. - [Cached Version]
  Published on: 10/15/2007    Last Visited: 10/21/2007  

  His colleague and co-author David H. Gutmann, M.D., Ph.D., the Donald O. Schnuck Family Professor of Neurology, specializes in NF1 research and directs the University's Neurofibromatosis Center, where the research took place.
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  Rubin and Gutmann decided to collaborate to see if that something was CXCL12, the protein that binds to CXCR4 to activate it.
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  "My lab had previously shown that loss of this gene made glia more likely to grow and divide, and now through this collaboration, we've learned how it also makes these cells more likely to survive, another step on the pathway to becoming cancerous," Gutmann says.
  
  Rubin and Gutmann have recently begun animal trials to see if a drug that elevates cAMP levels can inhibit tumor growth in Gutmann's mouse model of NF1.
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  "These are not new drugs, and they're known to be reasonably safe," Gutmann says.

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  brandywine.discoveryhospital.com/main.php?t=headlines&h - [Cached Version]
  Published on: 7/6/2005    Last Visited: 2/15/2007  

  This is yet another factor we need to consider when trying to understand how pediatric brain tumors form," study senior author Dr. David H. Gutmann, professor of neurology at Washington University School of Medicine in St. Louis, said in a prepared statement.
  
  He led six laboratories in a detailed genetic analysis of pilocytic astrocytoma, the most common kind of childhood brain tumor.
  
  "We were hoping to identify genes that contribute to the formation of these tumors and find indicators that might help us predict which tumors will be relatively well-behaved and which will be more aggressive," said Gutmann, who is also co-director of the neuro-oncology program at the Siteman Cancer Center.
  
  "When we looked at gene activity levels in the tumors as a function of brain location ... a very interesting pattern began to emerge," he said.
  
  The researchers found that tumors that develop in different parts of the brain retain distinct patterns of gene expression.This suggests that genetic fingerprints can be used to pinpoint the likely origins of brain tumors.
  
  The study is in the Feb. 1 issue of the journal Cancer Research.
  
  "There's been a movement in recent years to link normal brain development to pediatric neuro-oncology, and these findings affirm that as a necessary approach," Gutmann said.

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  www.lazyrussian.com/2007/02/13/genetics-and-brain-tumor - [Cached Version]
  Published on: 1/1/2007    Last Visited: 3/11/2007  

  Dr. David Gutmann, a Neuro-Oncologist at Washington University in St. Louis has been leading a study into the origins of tumors from a genetic perspective.

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  www.eurekalert.org/pub_releases/2007-04/wuso-btc041107. - [Cached Version]
  Published on: 4/11/2007    Last Visited: 4/13/2007  

  But senior author David Gutmann, M.D., Ph.D., the Donald O. Schnuck Family Professor of Neurology, says the findings also have implications for sporadic brain tumors, which affect many more people.
  
  "Until now, we've never really had a good system for studying how microglia may contribute to general brain tumor formation," says Gutmann, who is director of the Neurofibromatosis Center and co-director of the neuro-oncology program at the Siteman Cancer Center at Washington University and Barnes-Jewish Hospital.
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  "From a therapeutic standpoint, we're very focused in cancer therapy on poisoning the cancer cell," Gutmann says."But why not also deprive the cancer cell of the growth signals it receives from the normal surrounding tissue?These cells may actually decide whether a tumor forms at all and whether it continues to grow."
  
  To learn more about the neighboring cells' effects on brain tumors, Gutmann turned to NF1, which affects more than 100,000 people in the United States.Gutmann has studied the condition for years both to help improve NF1 treatment and to develop insights into brain tumors generally.As a part of that research, his lab developed a mouse model of NF1.
  
  Brain tumors in human patients and in the mouse model arise from brain support cells known as astrocytes.To begin the new study, Gutmann and his postdoctoral fellow Girish C. Daginakatte, Ph.D., studied these brain tumors early in their development to see if any other cell types were consistently nearby.
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  "I think people recognize now that microglia can be both good guys and bad guys," Gutmann says.
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  In a series of test tube experiments, Gutmann showed that hyaluronidase can promote astrocyte growth, and that inhibiting microglia production of hyaluronidase slowed their growth-promoting effects.
  
  "Now we have to wait for pharmaceutical scientists to develop inhibitors of hyaluronidase activity that can be used as potential treatments," Gutmann says.

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  www.jsmf.org/grants/d.php?id=2003022 - [Cached Version]
  Published on: 1/1/2003    Last Visited: 11/20/2008  

  Principal Investigator: David H. Gutmann, M.D., Ph.D.

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  www.omniomix.com/inthenews.php?id=75324 - [Cached Version]
  Published on: 4/11/2007    Last Visited: 4/17/2007  

  But senior author David Gutmann, M.D., Ph.D., the Donald O. Schnuck Family Professor of Neurology, says the findings also have implications for sporadic brain tumors, which affect many more people.
  
  "Until now, we've never really had a good system for studying how microglia may contribute to general brain tumor formation," says Gutmann, who is director of the Neurofibromatosis Center and co-director of the neuro-oncology program at the Siteman Cancer Center at Washington University and Barnes-Jewish Hospital.
  ...
  "From a therapeutic standpoint, we're very focused in cancer therapy on poisoning the cancer cell," Gutmann says."But why not also deprive the cancer cell of the growth signals it receives from the normal surrounding tissue?These cells may actually decide whether a tumor forms at all and whether it continues to grow."
  
  To learn more about the neighboring cells' effects on brain tumors, Gutmann turned to NF1, which affects more than 100,000 people in the United States.Gutmann has studied the condition for years both to help improve NF1 treatment and to develop insights into brain tumors generally.As a part of that research, his lab developed a mouse model of NF1.
  
  Brain tumors in human patients and in the mouse model arise from brain support cells known as astrocytes.To begin the new study, Gutmann and his postdoctoral fellow Girish C. Daginakatte, Ph.D., studied these brain tumors early in their development to see if any other cell types were consistently nearby.
  ...
  "I think people recognize now that microglia can be both good guys and bad guys," Gutmann says.
  ...
  In a series of test tube experiments, Gutmann showed that hyaluronidase can promote astrocyte growth, and that inhibiting microglia production of hyaluronidase slowed their growth-promoting effects.
  
  "Now we have to wait for pharmaceutical scientists to develop inhibitors of hyaluronidase activity that can be used as potential treatments," Gutmann says.

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